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http://purl.uniprot.org/citations/25695197http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25695197http://www.w3.org/2000/01/rdf-schema#comment"Beside its central role in the mitochondria-dependent cell death pathway, the apoptotic protease activating factor 1 (Apaf-1) is involved in the DNA damage response through cell-cycle arrest induced by genotoxic stress. This non-apoptotic function requires a nuclear translocation of Apaf-1 during the G1-to-S transition. However, the mechanisms that trigger the nuclear accumulation of Apaf-1 upon DNA damage remain to be investigated. Here we show that the main 4 isoforms of Apaf-1 can undergo nuclear translocation and restore Apaf-1 deficient MEFs cell cycle arrest in the S phase following genotoxic stress through activation of Chk-1. Interestingly, DNA damage-dependent nuclear accumulation of Apaf-1 occurs independently of p53 and the retinoblastoma (pRb) pathway. We demonstrated that Apaf-1 associates with the nucleoporin Nup107 and this association is necessary for Apaf-1 nuclear import. The CED-4 domain of Apaf-1 directly binds to the central domain of Nup107 in an ATR-regulated, phosphorylation-dependent manner. Interestingly, expression of the Apaf-1-interacting domain of Nup107 interfered with Apaf-1 nuclear translocation upon genotoxic stress, resulting in a marked reduction of Chk-1 activation and cell cycle arrest. Thus, our results confirm the crucial role of Apaf-1 nuclear relocalization in mediating cell-cycle arrest induced by genotoxic stress and implicate Nup107 as a critical regulator of the DNA damage-induced intra-S phase checkpoint response."xsd:string
http://purl.uniprot.org/citations/25695197http://purl.org/dc/terms/identifier"doi:10.1080/15384101.2015.1014148"xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/author"Villoutreix B.O."xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/author"Faye A."xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/author"Rain J.C."xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/author"Poyet J.L."xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/author"Bruzzoni-Giovanelli H."xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/author"Jagot-Lacoussiere L."xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/name"Cell Cycle"xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/pages"1242-1251"xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/title"DNA damage-induced nuclear translocation of Apaf-1 is mediated by nucleoporin Nup107."xsd:string
http://purl.uniprot.org/citations/25695197http://purl.uniprot.org/core/volume"14"xsd:string
http://purl.uniprot.org/citations/25695197http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25695197
http://purl.uniprot.org/citations/25695197http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25695197
http://purl.uniprot.org/uniprot/#_B3KMK0-mappedCitation-25695197http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25695197
http://purl.uniprot.org/uniprot/#_G3V1T4-mappedCitation-25695197http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25695197
http://purl.uniprot.org/uniprot/#_P57740-mappedCitation-25695197http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25695197
http://purl.uniprot.org/uniprot/P57740http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25695197
http://purl.uniprot.org/uniprot/G3V1T4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25695197
http://purl.uniprot.org/uniprot/B3KMK0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25695197